Bacterial infections in Guillain-Barré and Fisher syndromes

Abstract

Progress has been made in our understanding of Guillain-Barré syndrome, especially in identifying the Campylobacter jejuni genes responsible for the development of clinical features. C. jejuni is grouped into several classes based on the organization of lipo-oligosaccharide biosynthesis genes. A specific class carrying a sialyltransferase gene (cst-II) is associated with the development of Guillain-Barré syndrome, which is essential for the biosynthesis of ganglioside-like lipo-oligosaccharides. The class of C. jejuni expressed both GM1-like and GD1a-like lipo-oligosaccharides, which could induce the production of autoantibodies to GM1, to GD1a or to the GM1/GD1a complex, possibly increasing the risk of development. C. jejuni sialyltransferase (Cst-II) consists of 291 amino acids, and the 51st amino acid determines its enzymatic activity. Strains with cst-II (Thr51) expressed GM1-like or GD1a-like lipo-oligosaccharide whereas strains with cst-II (Asn51) expressed GT1a-like or GD1c-like lipo-oligosaccharide. Patients infected with the cst-II (Thr51) strains had anti-GM1 or anti-GD1a IgG antibodies, and showed limb weakness. Patients infected with the cst-II (Asn51) strains had anti-GQ1b IgG antibodies, and showed ophthalmoplegia and ataxia. The cst-II gene is responsible for the development of Guillain-Barré and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis.